Evidence map›Paper›PMID 32664576›Full record

ReviewInternational journal of molecular sciences2020

Ferroptosis in Liver Diseases: An Overview.

Martina Maria Capelletti, Hana Manceau, Hervé Puy, Katell Peoc'h

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
200citing papers in PubMed, 3 pooled it
26.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

200 citing papers in PubMed, 3 syntheses or guidelines pooled it, 347 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Ferroptosis in heatstroke: Mechanisms and therapeutic perspectives (Review).International journal of molecular medicine · 2026
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Low 5HTJournal of neurochemistry · 2026
    Review
  15. Review
  16. Review
  17. Article
  18. PMEnvironment & health (Washington, D.C.) · 2026
    Article
  19. Article
  20. Review

140 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 2 countries.

Martina Maria CapellettiCentre de Recherche sur l'Inflammation, INSERM U1149, Université de Paris, Laboratory of Excellence GR-Ex, 75018 Paris, France.ORCID 0000-0003-2699-9126
Hana ManceauCentre de Recherche sur l'Inflammation, INSERM U1149, Université de Paris, Laboratory of Excellence GR-Ex, 75018 Paris, France.
Hervé PuyCentre de Recherche sur l'Inflammation, INSERM U1149, Université de Paris, Laboratory of Excellence GR-Ex, 75018 Paris, France.
Katell Peoc'hCentre de Recherche sur l'Inflammation, INSERM U1149, Université de Paris, Laboratory of Excellence GR-Ex, 75018 Paris, France.
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is an iron-dependent form of cell death characterized by intracellular lipid peroxide accumulation and redox imbalance. Ferroptosis shows specific biological and morphological features when compared to the other cell death patterns. The loss of lipid peroxide repair activity by glutathione peroxidase 4 (GPX4), the presence of redox-active iron and the oxidation of polyunsaturated fatty acid (PUFA)-containing phospholipids are considered as distinct fingerprints of ferroptosis. Several pathways, including amino acid and iron metabolism, ferritinophagy, cell adhesion, p53, Keap1/Nrf2 and phospholipid biosynthesis, can modify susceptibility to ferroptosis. Through the decades, various diseases, including acute kidney injury; cancer; ischemia-reperfusion injury; and cardiovascular, neurodegenerative and hepatic disorders, have been associated with ferroptosis. In this review, we provide a comprehensive analysis of the main biological and biochemical mechanisms of ferroptosis and an overview of chemicals used as inducers and inhibitors. Then, we report the contribution of ferroptosis to the spectrum of liver diseases, acute or chronic. Finally, we discuss the use of ferroptosis as a therapeutic approach against hepatocellular carcinoma, the most common form of primary liver cancer.

Indexed as

Ferroptosisalpha-TocopherolAnimalsAutophagyChemical and Drug Induced Liver InjuryCyclohexylaminesCysteineGlutathioneHemeHumansIronKelch-Like ECH-Associated Protein 1Lipid PeroxidationLipoxygenaseLiver DiseasesLiver Neoplasmsalpha-TocopherolCyclohexylaminesCysteineerastinferrostatin-1GlutathioneHemeIronKEAP1 protein, humanKelch-Like ECH-Associated Protein 1Lipoxygenaseliproxstatin-1PhenylenediaminesPhospholipid Hydroperoxide Glutathione PeroxidasePiperazinesQuinoxalinesReactive Oxygen SpeciesSorafenibSpiro CompoundsSulfasalazineTP53 protein, humanTumor Suppressor Protein p53cell deathferroptosisiron metabolismliver

Identifiers

PMID32664576
PMCPMC7404091
OpenAlexW3041185009

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.